长期运动性疲劳与运动缺乏对Wistar大鼠神经内分泌系统的不同影响

目的: 观察长期运动性疲劳与运动缺乏2种不同状态对机体神经内分泌系统的影响。方法: 60只雄性Wistar大鼠随机分为3组:正常对照组、运动性疲劳模型组、运动缺乏模型组,每组20只。采用“基础饮食复合负重游泳”方法(2周)建立运动性疲劳大鼠模型;采用“限制活动”方法建立运动缺乏大鼠模型,时间共计10周。实验结束后测定大鼠爬杆时间、双抗夹心ELISA法测定各组大鼠下丘脑促甲状腺激素释放激素(thyrotropin-releasing hormone,TRH)及血清去甲肾上腺素(norepinephrine,NE)、肾上腺素(epinephrin,E)含量;放射免疫均相竞争法测定下丘脑促肾上腺皮质激素释放激素(corticotropin releasing hormone,CRH)、垂体促肾上腺皮质激素(adrenocorticotrophic hormone,ACTH)与促甲状腺激素(thyroid stimulating hormone,TSH)以及血清皮质酮(corticosterone,CORT)、三碘甲腺原氨酸(triiodothyronine, T3)、甲状腺素(tetraiodothyronine,T4)含量,以评价交感神经－肾上腺髓质系统、下丘脑-垂体-肾上腺(hypothalamic-pituitary-adrenocortical, HPA)轴、下丘脑-垂体-甲状腺(hypothalamo-pituitary-thyroid, HPT)轴功能。结果: 2模型组大鼠爬杆时间明显缩短;运动性疲劳模型组大鼠交感神经－肾上腺髓质系统与HPA轴功能抑制,HPT轴无变化;运动缺乏模型组大鼠HPA轴功能亢进、HPT轴功能抑制,交感神经－肾上腺髓质系统无变化。结论: 长期运动性疲劳与运动缺乏均能影响机体神经内分泌系统,导致其调节机制失衡,但二者的作用靶标及趋势不同。     

Increased plasma miR-146a levels are associated with subclinical atherosclerosis in newly diagnosed type 2 diabetes mellitus

AimsThe association between circulating miR-146a and subclinical atherosclerosis in type 2 diabetes mellitus (T2DM) remains poorly understood. This study aimed to investigate the correlation between plasma miR-146a levels and subclinical atherosclerosis as measured by the carotid intima-media thickness (CIMT) and brachial-ankle pulse wave velocity (baPWV) in patients with newly diagnosed T2DM.MethodsWe studied 100 patients with newly diagnosed T2DM. Subclinical atherosclerosis was defined as a thickened CIMT (≥1.0 mm) and high baPWV defined as a value greater than the 75th percentile. Plasma miR-146a levels and metabolic parameters were measured.ResultsPatients with thickened CIMT had higher plasma miR-146a levels than those without thickened CIMT (3.36 ± 1.32 vs 1.38 ± 1.11, P < 0.001). Patients in the high baPWV group had higher plasma miR-146a levels than those in the normal baPWV group (3.43 ± 1.32 vs 1.98 ± 1.48, P < 0.001). Both CIMT (β = 0.569, P < 0.001) and baPWV (β = 0.274, P = 0.001) positively correlated with plasma miR-146a levels after adjustment for confounding factors by multiple stepwise regression. On binary logistic regression, plasma miR-146a level was an independent risk factor for thickened CIMT (OR = 3.890, 95% CI 1.415–7.698, P = 0.008) and high baPWV (OR = 1.954, 95% CI 1.256–3.040, P = 0.002) after adjustment for established cardiovascular risk factors. The area under the receiver operating characteristics curve (AUROC) of plasma miR-146a level for predicting thickened CIMT was 0.795 (95%CI 0.708–0.883, P < 0.001) and for predicting high baPWV was 0.773 (95%CI 0.679–0.867, P < 0.001).ConclusionPlasma miR-146a levels correlate with CIMT and baPWV and could act as a biomarker for early diagnosis and as a therapeutic target for atherosclerosis in T2DM.     

Comfortable lifestyle-induced imbalance of neuro-endocrineimmunity network: A possible mechanism of vascular endothelial dysfunction

<正>Objective:To observe the changes of vascular endothelial functions and general neuroendocrine -immunity(NEI) network under the state of qi-deficiency syndrome induced by excessive idleness and to approach their internal relevance and illuminate initially the pathophysiological mechanism of vascular lesion induced by excessive idleness.Methods:A total of 100 male Wistar rats were randomly divided into the control group and the qi-deficiency syndrome model group,50 rats in each group.The qi-deficiency syndrome model was established by feeding the animals with hyper-alimentation diet in combination with restricting movement for 10 weeks.Changes of common chemical signal molecules related to NEI and vascular endothelial functions were measured by the end of the experiment.Furthermore,their internal relevance was analyzed by the method of canonical correlation analysis.Results:The vascular endothelial structure and function were obviously injured in the model group.Compared with the control group,the chemical signal molecules,such as 5-hydroxytryptamine (5-HT),corticosterone(CORT),triiodothyronine(T3),tetraiodothyronine(T4),angiotensinⅡ(AngⅡ), interleukin-1(IL-1),and tumor necrosis factor-α(TNF-α) in peripheral blood of the model group(n=43) were changed significantly(P0.05 or P0.01).Canonical correlation analysis showed that vascular endothelial dysfunction was correlated to the changes of these signal molecules in the NEI network.Conclusions:Comfortbased lifestyle induced not only vascular endothelial dysfunction but also an imbalance of the NEI network. Vascular endothelial dysfunction and the imbalanced NEI network interacted with each other,and an imbalance of the NEI network may be the pathophysiologic basis for the genesis and development of vascular endothelial dysfunction,even diseases of the blood vessel.